Gene Point Mutations Are Not Antifungal Resistance Markers in .

The high rates of antifungal resistance in may be facilitated by the presence of alterations in the gene. We aimed to study the sequence of the gene in 124 invasive isolates causing incident episodes of candidemia ( = 81), subsequent candidemia episodes ( = 9), endocarditis ( = 2), and -generated echinocandin-resistant isolates ( = 32) and assessed its relationship with genotypes, acquisition of antifungal resistance and , and patient prognosis. The gene was sequenced, and isolates were genotyped using six microsatellite markers and multilocus sequence typing (MLST) based on six housekeeping genes. According to EUCAST, isolates causing candidemia ( = 90) were echinocandin susceptible, and four of them were fluconazole resistant (MIC ≥64 mg/liter). One isolate obtained from a heart valve was resistant to micafungin and anidulafungin (MICs, 2 mg/liter and 1 mg/liter, respectively). gene mutations were present in 44.4% of the incident isolates, the most common being V239L. The presence of mutations was not correlated with or antifungal resistance. Microsatellite and MLST revealed 27 genotypes and 17 sequence types, respectively. Fluconazole-resistant isolates were unrelated. Most mutations were found in cluster isolates; conversely, some mutations were found in more than one genotype. No clinical differences, including previous antifungal use, were found between patients infected by wild-type gene isolates and isolates with any point mutation. The presence of gene mutations in isolates causing candidemia is not correlated with specific genotypes, the promotion of antifungal resistance, or the clinical outcome.